Equine motor neuron disease (EMND) is a relatively new condition that affects the nervous and muscular systems in adult horses.
It was first diagnosed in the US in 1990 in New York state, and has also been diagnosed as far west as the state of Oregon.
It is most prevalent in the US, and to date, fewer than 200 horses have been diagnosed with EMND.
Affected horses demonstrate marked weight loss in the face of a ravenous appetite. This weight loss is attributed to neurogenic muscular atrophy. Presently there is no know cause of the disease.
A horse with this condition appears with muscle tremors, and may appear to be “tied up,” (short-strided gait). Other signs may include constant shifting of weight in the rear limbs and abnormally low head carriage. The horse also has a particular stance, with all four limbs camped (tucked) under.
The condition usually progresses with continued muscle atrophy and debilitation over the course of one to several months. Occasionally the condition will stabilize or even seem to improve one to two months after the onset. Following this period in many horses, the condition becomes progressive, requiring euthanasia.
A few horses have stabilized for as long as three years, however, none have returned to effective use.
The horse characteristically has mild elevations of the muscle-derived enzymes, CPK and AST. Electromyography (EMG) is frequently used as an aid in the diagnosis of this condition. Although there is no definitive diagnostic test available for this condition, the clinical signs, changes in muscle enzymes and EMG findings provide strong support for the diagnosis of EMND. Muscle and nerve biopsies have characteristic findings of EMND.
A definitive cause for EMND has not been determined; a common toxin has not been identified and infectious agents are not likely because of the sporadic nature of the disease. Horses without access to pasture seem to be at higher risk for developing the disease.
Although speculative, it is suggested that some oxidative injury may cause the neuronal cell death leading to the clinical signs. Vitamin E is a dietary antioxidant which may be useful in halting the progression of the disease.
Trembling – muscle tremors and fasciculations.
Excessive periods of recumbency.
Abnormal limb positioning – weight onto rear legs and hold all 4 limbs closer together than normal.
Weakness without ataxia.
Appetite remains normal – normal gut motility.
Malabsorption of nutrients from the gut suggests that absorptive function of the gut is abnormal → abnormal function.
Symmetrical muscle atrophy, especially in triceps , scapula, quadriceps, lumbar , sacral and neck muscles.
Stabilization in 2-8 weeks to arrested form.
Symmetrical buckling of forelimbs while standing.
Abnormally low head carriage.
Elevation of tailhead.
Cranial nerve deficits.
Persistent recumbency, respiratory distress.
Failure to gain weight despite normal appetite.
Abnormal gait – stumbling, stringhalt-like in several limbs.
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Clinical signs information from Vetstream